Knockdown of miR-155 alleviates skin damage in rats with chronic spontaneous urticaria by modulating the JAK/STAT signaling pathway.

IF 2.6 4区医学 Q2 ALLERGY

Allergy Asthma and Clinical Immunology Pub Date : 2024-06-29 DOI:10.1186/s13223-024-00902-x

Yue-Peng An, Rui Yuan, Shan-Shan Wang, Su-Qing Yang, Qing Zhang

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Abstract

Objective: The aim of this study was to investigate the role and mechanisms of miR-155 in chronic spontaneous urticaria (CSU).

Methods: The expression level of miR-155 in the skin tissues of patients with CSU and experimental rats were detected by RT-qPCR, followed by the measurement of the histamine release rate in the serum through the histamine release test. Besides, hematoxylin & eosin staining was used to observe the pathological changes of the skin tissues; Corresponding detection kits and flow cytometry to measure the changes of immunoglobulins, inflammatory cytokines and T cell subsets in the serum of rats in each group; and western blot to check the expression level of proteins related to JAK/STAT signaling pathway in the skin tissues.

Results: Knockdown of miR-155 reduced the number and duration of pruritus, alleviated the skin damage, and decreased the number of eosinophils in CSU rats. Moreover, knockdown of miR-155 elevated the serum levels of IgG and IgM, decreased the levels of IgA and inflammatory cytokines, and reduced the proportion of CD4 + and CD4 + CD25 + T cells, as well as the CD4+/CD8 + ratio in CSU rats. However, Tyr705 intervention could reverse the effects of knockdown of miR-155 on CSU model rats. Furthermore, we found that knockdown of miR-155 significantly reduced the protein expression of IRF-9, as well as the P-JAK2/JAK2 and P-STAT3/STAT3 ratios in the skin tissues of CSU rats.

Conclusion: Knockdown of miR-155 can alleviate skin damage and inflammatory responses and relieve autoimmunity in CSU rats by inhibiting the JAK/STAT3 signaling pathway.

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通过调节 JAK/STAT 信号通路敲除 miR-155 减轻慢性自发性荨麻疹大鼠的皮肤损伤

研究目的本研究旨在探讨miR-155在慢性自发性荨麻疹（CSU）中的作用和机制：方法：采用RT-qPCR技术检测miR-155在慢性自发性荨麻疹患者和实验鼠皮肤组织中的表达水平，并通过组胺释放试验测定血清中组胺的释放率。此外，还采用苏木精和伊红染色法观察皮肤组织的病理变化；采用相应的检测试剂盒和流式细胞术检测各组大鼠血清中免疫球蛋白、炎症细胞因子和T细胞亚群的变化；采用Western blot检测皮肤组织中JAK/STAT信号通路相关蛋白的表达水平：结果：敲除 miR-155 能减少 CSU 大鼠瘙痒的数量和持续时间，减轻皮肤损伤，减少嗜酸性粒细胞的数量。此外，敲除 miR-155 会升高 CSU 大鼠血清中 IgG 和 IgM 的水平，降低 IgA 和炎性细胞因子的水平，并降低 CD4 + 和 CD4 + CD25 + T 细胞的比例以及 CD4 +/CD8 + 的比率。然而，Tyr705的干预可以逆转敲除miR-155对CSU模型大鼠的影响。此外，我们还发现，敲除 miR-155 能显著降低 CSU 大鼠皮肤组织中 IRF-9 蛋白表达以及 P-JAK2/JAK2 和 P-STAT3/STAT3 比率：结论：敲除 miR-155 可以通过抑制 JAK/STAT3 信号通路减轻 CSU 大鼠的皮肤损伤和炎症反应，缓解自身免疫。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Allergy Asthma and Clinical Immunology ALLERGY-IMMUNOLOGY

CiteScore

4.30

自引率

3.70%

发文量

审稿时长

12 weeks

期刊介绍： Allergy, Asthma & Clinical Immunology (AACI), the official journal of the Canadian Society of Allergy and Clinical Immunology (CSACI), is an open access journal that encompasses all aspects of diagnosis, epidemiology, prevention and treatment of allergic and immunologic disease. By offering a high-visibility forum for new insights and discussions, AACI provides a platform for the dissemination of allergy and clinical immunology research and reviews amongst allergists, pulmonologists, immunologists and other physicians, healthcare workers, medical students and the public worldwide. AACI reports on basic research and clinically applied studies in the following areas and other related topics: asthma and occupational lung disease, rhinoconjunctivitis and rhinosinusitis, drug hypersensitivity, allergic skin diseases, urticaria and angioedema, venom hypersensitivity, anaphylaxis and food allergy, immunotherapy, immune modulators and biologics, immune deficiency and autoimmunity, T cell and B cell functions, regulatory T cells, natural killer cells, mast cell and eosinophil functions, complement abnormalities.